Hippocampal long-term potentiation in vivo induces translocation of protein kinase Cγ

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Abstract
The possible involvement of the Ca2+-dependent protein kinase C (PKC) isoenzymes α/β and γ in mechanisms of long-term potentiation (LTP) was investigated after tetanic stimulation of the perforant path in vivo. Brief tetanic stimulation of the perforant path resulted in a 150% increase in population spike amplitude recorded from the dentate gyrus synapses in response to test stimuli 5 and 10 min after tetanization. Immunoblot analysis of PKC immunoreactivity in cytosolic and membrane fractions revealed a LTP-induced translocation of γ PKC but not α/β PKC into the cytosol in dentate gyrus but also in the other ipsilateral hippocampal regions. These data suggest different physiological roles of Ca2+-dependent PKC isoenzymes in activity-dependent synaptic plasticity.